Martínez-Abarca Millán, A.; Soler Beatty, J.; Valencia Expósito, A.; Martín-Bermudo, M.D. Drosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins. Genes2023, 14, 1502.
Martínez-Abarca Millán, A.; Soler Beatty, J.; Valencia Expósito, A.; Martín-Bermudo, M.D. Drosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins. Genes 2023, 14, 1502.
Martínez-Abarca Millán, A.; Soler Beatty, J.; Valencia Expósito, A.; Martín-Bermudo, M.D. Drosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins. Genes2023, 14, 1502.
Martínez-Abarca Millán, A.; Soler Beatty, J.; Valencia Expósito, A.; Martín-Bermudo, M.D. Drosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins. Genes 2023, 14, 1502.
Abstract
Oncogenic mutations in the small GTPase Ras contributes to ~30% of human cancers. However, tissue growth induced by oncogenic Ras is restrained by induction of cellular senescence and additional mutations are required to induce tumor progression. Therefore, it is paramount to identify cooperating cancer genes. Recently, the tensin family of focal adhesion proteins, TNS1-4, have emerged as regulators of carcinogenesis, yet their role in cancer appears somewhat controversial. Around 90% of human cancers are of epithelial origin. We have used the Drosophila wing imaginal disc epithelium as model system to gain insight into the roles of two orthologs of human TNS2 and 4, blistery (by) and PVRAP, in epithelial cancer progression. We have generated null mutations in PVRAP and found that, as it is the case for by and mammalian tensins, PVRAP mutants are viable. We have also found that elimination of either PVRAP or by potentiates RasV12-mediated wing disc hyperplasia. Furthermore, our results have unravelled a mechanism by which tensins may limit Ras oncogenic capacity, the regulation of cell shape and growth. These results demonstrate that Drosophila tensins behave as suppressors of Ras-driven tissue hyperplasia, suggesting that the roles of tensins as modulators of cancer progression might be evolutionary conserved.
Keywords
oncogenic Ras, overgrowth, tensins, Drosophila
Subject
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
